Eating Animals by Jonathan Safran Foer

[JaneV2.0]

"In Malcolm Gladwell's book Outliers, he starts off by talking about a small Italian community in PA that is extremely long-lived and he talks about how a doctor and a sociologist went there to try to get the secret of their long, healthy lives. He started at the logical place, diet and exercise. But they learned that 41% of the community's diet was fat. Most of them smoked, and they struggled with obesity. To make a long story short, they concluded it was their community, tradition, their practice of walking from house to house and speaking with each other, and their affiliation with organizations and community groups that kept them alive so long. So there are too many variables really to come up with the definitive formula for health."

Roseto. As I recall, once they spread out into the population and got caught up in modern stressors, their offspring started getting just as sick as the rest of us. My oft-stated theory is that illness begins where genes and stress meet, and this community seems to back that up. It's another reason I get so tired of the constant browbeating of smokers and fat people. The bullies are missing the point. Scapegoating people and making pariahs out of them is at least as likely to make them sick as their body shape or habits will.

[JaneV2.0]

"In the end, is it really a matter of trusting your own gut and instinct??? "

I think you read and consider, observe the world around you, consult your gut, and move in that direction. The folly of making science your god and sneering at instinct/intuition/unmeasurable variables is that science is generally a lot more corrupt and fallible than your instincts are. IMO.

And I do agree with Ravnskov (and my mother) that you're going to die of something, no matter how obsessive you may be about your health. Worrying about every sneeze and pimple will likely hasten your inevitable demise.

[kib]

Ya ya, we are. But if 25% of premature death is caused by heart disease that could be easily prevented, even if only 5% of the population dies prematurely, why not incorporate it?

I just got irked, because his ideas / criticisms seemed logical and unbiased and I was patiently ignoring the horrendous grammatical and editing errors that usually goes hand in hand with tracts-from-wackos, and then he mentions as an aside on the last page that his potential conflict of interest, which he has harped on endlessly as a problem with other researchers' positions, is positively gargantuan. It doesn't necessarily negate his work, but it certainly puts a big question mark on it.

[JaneV2.0]

It's been awhile since I read Ravnskov, and then mostly articles--though I think I have his latest book--but if I'm interpreting what you say correctly, he may consider the public health implications (macro) less compelling than the physiological ones (micro). I always follow the money, and I doubt he's making much, so I wouldn't worry about this being a conflict of interest.

Also, re statins, you can lower inflammation by avoiding inflammatory substances (including sugar and starchy carbohydrates), by supplementing with B-vitamins (which are consumed by same), by stress-reduction techniques, and probably by regular low-intensity exercise. When triglycerides are brought down this way, LDL generally follows, but if numbers concern you, you can have particle size checked with a VAP test. So-called "large, fluffy" particles are considered harmless. So why take a sledgehammer approach with Lipitor and risk brain damage (see Duane Graveline) or muscle wasting, among other risks.

Re The China Study, Denise Minger does a dazzling (and mind-twisting for those of us disinclined toward statistical analysis) refutation of his tortured findings. Well worth spending time with.

[kib]

With Ravnskov, I have to wonder ... I believe a lot of the book is a reiteration of his work in Cholesterol Myths. The quality of his analyses only took a nosedive toward the end, where his tone became rather peevish and bitter and his criticisms went from sharp scientific objections to vague harping.

Amazing, that's the third time in two days Graveline has come up in my world. He's the one with the explanation that statins inhibit inflamation-essential NF-bk, and that is the reason they do actually have a positive effect on CHD mortality, it's got nothing to do with cholesterol reduction. This fits so well with the theory of atheroma and vulnerable plaque it made my hair stand up. In one bizzare moment I thought ... heart attack is nothing but the bursting of arterial zits, and grandma was right: sugar gives you pimples.

Perhaps not my most brilliant scientific moment, but I have a feeling there's a grain of truth (and monocyte-engulfed-LDL-bonded bacteria) in there somewhere.

[JaneV2.0]

It sounds good to me. I wrote a recent post about scientific breakthroughs being mostly inspiration--sometimes influenced by psychoactive drugs --and I think your heart-zit theory resonates nicely with that.

[kib]

Well the mechanism of some (all?) heart attacks is almost exactly that, this boil (a "vulnerable plaque") on the artery wall that develops over a cholesterol plaque ("atheroma") inside the wall finally gives way and bursts, releasing chunks of endothelial cells, a pudding-like blob of pus, a thick lump of sebumlike ldl/bacteria, and a tiny bit of blood. The body senses injury and works to create a clot to repair it. This sudden accumulation of glop/clot creates a coronary blockage and results in heart muscle death.

The question is, what's the mechanism that causes the original atheroma, and why can it simply accumulate, causing atherosclerosis but no overt disease, in some people, while it becomes an active inflamed "zit" that causes a heart attack in others. Is the arterial wall damaged, the LDL molecules slip under it and then an infection eventually results? Is the wall damaged and bacteria get in and then the LDL molecules follow to combat the bacteria and get trapped? If so, what damages the arterial wall in the first place? Glucose? Insulin? Fatty Acids? Cortisol? Something else? All of the above? Or is the bonded bacteria and LDL coming in from the other side of the artery, the vasa vasorum, trying to pass naturally through the artery and out of the body and getting stuck in the artery wall for some reason? What is the trigger that causes inflamation of that stuck lump of molecules (or allows it to remain inert)?

The question is: do these atheromas inflame and burst all the time, but only cause a heart attack if they clot fast enough to occlude the artery? That might explain why it's so hard to pinpoint a biochemical difference between heart attack patients and angina patients : the mechanism's exactly the same, heart attack victims just had the bad luck - fast clotting, bigger atheroma or more pus, unfortunate placement of the endothelial flap - to clog the artery. ???


Inquiring minds want to know!!! ... inquiring minds should probably go take a shower already ....

[JaneV2.0]

Perhaps a nap would be more productive. You wouldn't be the first inquiring mind who dreamed the solution to a vexing problem.

As far as "what makes the difference?" Lazy thinker that I am, I'd just go back to "genes plus stress." There are assaults, infections, and repair going on all the time inside us, with bodily defenses doing their job and us all unknowing. I figure the best I can do is minimize stressors and not get in the way of the cleanup crew.

[kib]

Maybe it really is stress, even from a biochemical perspective. Maybe any "sharp" molecule not supposed to be eternally circulating in high levels in the blood, whether it's glucose or cortisol or the remains of howdy doody, eventually causes damage to that raised endothelium over an atheroma. Hmmm.

I divorced Jerry Seinfeld last night because I really just wasn't that into him and frankly he was annoying me and I finally understood that he really wanted to date George. Somehow my naps aren't quite as insightful as the rest of my hours.